Source:http://linkedlifedata.com/resource/pubmed/id/20586818
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2010-11-16
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pubmed:abstractText |
Interferon-? (IFN-?) has a direct role in thyroid destruction in autoimmune thyroiditis. Interleukin-18 (IL-18), a pro-inflammatory cytokine with potent IFN-? inducing activities, may play an important role in Th1-mediated autoimmune diseases. The purpose of this study was to characterize the expression and localization of IL-18 in the thyroid tissues of Hashimoto's thyroiditis (HT) and to investigate the effect of IFN-? on IL-18 expression in isolated human thyroid follicular cells (TFCs). Thyroid tissues obtained from six euthyroid patients with HT and six control subjects were used to detect IL-18 expression by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical staining. Human TFCs were isolated and incubated for 48 h with or without IFN-?, tumour necrosis factor-? (TNF-?) or IL-1?. IL-18 expression was analysed by RT-PCR, immunofluorescent double staining and western blot. We found that IL-18 expression was increased in the thyroid tissues of HT compared with control thyroid tissues. TFCs were major cell types expressing IL-18 in the thyroid tissues of HT. IL-18 was constitutively expressed in isolated human TFCs, and the expression was significantly up-regulated by IFN-? rather than TNF-? or IL-1?. Western bolt revealed that a 24-kDa band corresponding to pro-IL-18 was broadened in the lysates of IFN-?-treated TFCs. Our results demonstrated that IL-18 expression is up-regulated in the TFCs of HT patients and in primary human TFCs exposed to IFN-?. Therefore, intrathyroidal interaction between IL-18 and IFN-? may have a role in promoting the local immune response, which contributes to the thyroid destruction seen in HT.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1365-2613
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pubmed:author | |
pubmed:copyrightInfo |
© 2010 The Authors. Journal compilation © 2010 Blackwell Publishing Ltd.
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pubmed:issnType |
Electronic
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pubmed:volume |
91
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
420-5
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pubmed:meshHeading |
pubmed-meshheading:20586818-Adult,
pubmed-meshheading:20586818-Biopsy,
pubmed-meshheading:20586818-Cells, Cultured,
pubmed-meshheading:20586818-Female,
pubmed-meshheading:20586818-Gene Expression,
pubmed-meshheading:20586818-Hashimoto Disease,
pubmed-meshheading:20586818-Humans,
pubmed-meshheading:20586818-Interferon-gamma,
pubmed-meshheading:20586818-Interleukin-18,
pubmed-meshheading:20586818-Interleukin-1beta,
pubmed-meshheading:20586818-Male,
pubmed-meshheading:20586818-Middle Aged,
pubmed-meshheading:20586818-Thyroid Gland,
pubmed-meshheading:20586818-Tumor Necrosis Factor-alpha,
pubmed-meshheading:20586818-Up-Regulation
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pubmed:year |
2010
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pubmed:articleTitle |
Thyrocyte interleukin-18 expression is up-regulated by interferon-? and may contribute to thyroid destruction in Hashimoto's thyroiditis.
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pubmed:affiliation |
Department of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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